From Vascular Smooth Muscle Cells to Folliculogenesis: What About Vasorin?

Bonnet, Anne‐Laure; Miller, Catherine; Broutin, Isabelle; Rochefort, Gaël Y.; Schrewe, Heinrich; Gaucher, Céline

doi:10.3389/fmed.2018.00335

Cited by 22 publications

(36 citation statements)

References 23 publications

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“… 36 VASN deficiency causes unknown death within 3 weeks. 7 Our data corresponded with those in previous studies showing sudden death in young VASN −/− mice (Figure 2 ). Our unpublished studies also showed that VASN deficiency induces inflammation and pathology in the lung, kidney and liver.…”

Section: Discussionsupporting

confidence: 93%

“… 6 Soluble VASN protein can bind to TGF‐β, which can inhibit epithelial‐to‐mesenchymal transition. 7 A previous study showed high VASN expression in human glioblastoma in the context of TNF α‐induced apoptosis. 7 CRISPR/Cas9 technology could be used to generate a knockout mouse model to further study the function of VASN and its associated signalling pathway.…”

Section: Introductionmentioning

confidence: 97%

“… 7 CRISPR/Cas9 technology could be used to generate a knockout mouse model to further study the function of VASN and its associated signalling pathway. However, unexplained death occurs in VASN −/− mice shortly after birth, 7 and it was unclear whether this phenomenon was related to heart damage.…”

Section: Introductionmentioning

confidence: 99%

“…However, unexplained death occurs in VASN −/− mice shortly after birth, 7 and it was unclear whether this phenomenon was related to heart damage.…”

mentioning

confidence: 99%

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Vasorin deficiency leads to cardiac hypertrophy by targeting MYL7 in young mice

Guo

Liang

et al. 2021

J Cellular Molecular Medi

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Vasorin (VASN), also known as SLIT-like 2 (slitl2), is a 673-amino acid transmembrane glycoprotein localized on the cell surface 1 that is cleaved by a disintegrin and metalloproteinase. VASN is considered a potential biomarker and therapeutic target for cancer. 2,3 Notably, VASN is highly conserved in many organs from embryonic development to adulthood. 4,5 There is limited literature on VASN function.In embryonic development, VASN is primarily expressed in the heart and lungs. 1 VASN is expressed in vascular smooth muscle cells 1 and

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

“…However, unexplained death occurs in VASN −/− mice shortly after birth, 7 and it was unclear whether this phenomenon was related to heart damage.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Vasorin deficiency leads to cardiac hypertrophy by targeting MYL7 in young mice

Guo

Liang

et al. 2021

J Cellular Molecular Medi

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“…For instance, vasorin (VASN) was found to modulate arterial response to injury in vivo [ 38 ]. It also appears to be involved in cellular migration and proliferation/differentiation [ 39 ]. Neural cell adhesion molecule-1 (NCAM1) is involved in cell–cell and matrix adhesion in cardiomyocytes adhesion [ 40 ], and is upregulated under metabolic stress [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Lipoprotein Proteomics and Aortic Valve Transcriptomics Identify Biological Pathways Linking Lipoprotein(a) Levels to Aortic Stenosis

et al. 2021

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Lipoprotein(a) (Lp(a)) is one of the most important risk factors for the development of calcific aortic valve stenosis (CAVS). However, the mechanisms through which Lp(a) causes CAVS are currently unknown. Our objectives were to characterize the Lp(a) proteome and to identify proteins that may be differentially associated with Lp(a) in patients with versus without CAVS. Our second objective was to identify genes that may be differentially regulated by exposure to high versus low Lp(a) levels in explanted aortic valves from patients with CAVS. We isolated Lp(a) from the blood of 21 patients with CAVS and 22 volunteers and performed untargeted label-free analysis of the Lp(a) proteome. We also investigated the transcriptomic signature of calcified aortic valves from patients who underwent aortic valve replacement with high versus low Lp(a) levels (n = 118). Proteins involved in the protein activation cascade, platelet degranulation, leukocyte migration, and response to wounding may be associated with Lp(a) depending on CAVS status. The transcriptomic analysis identified genes involved in cardiac aging, chondrocyte development, and inflammation as potentially influenced by Lp(a). Our multi-omic analyses identified biological pathways through which Lp(a) may cause CAVS, as well as key molecular events that could be triggered by Lp(a) in CAVS development.

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Enhanced vasorin signaling mitigates adverse cardiovascular remodeling

Wang,

McGraw,

Monticone

et al. 2024

Aging Medicine

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Arterial stiffening is a critical risk factor contributing to the exponential rise in age‐associated cardiovascular disease incidence. This process involves age‐induced arterial proinflammation, collagen deposition, and calcification, which collectively contribute to arterial stiffening. The primary driver of proinflammatory processes leading to collagen deposition in the arterial wall is the transforming growth factor‐beta1 (TGF‐β1) signaling. Activation of this signaling is pivotal in driving vascular extracellular remodeling, eventually leading to arterial fibrosis and calcification. Interestingly, the glycosylated protein vasorin (VASN) physically interacts with TGF‐β1, and functionally restraining its proinflammatory fibrotic signaling in arterial walls and vascular smooth muscle cells (VSMCs). Notably, as age advances, matrix metalloproteinase type II (MMP‐2) is activated, which effectively cleaves VASN protein in both arterial walls and VSMCs. This age‐associated/MMP‐2‐mediated decrease in VASN levels exacerbates TGF‐β1 activation, amplifying arterial fibrosis and calcification in the arterial wall. Importantly, TGF‐β1 is a downstream molecule of the angiotensin II (Ang II) signaling pathway in the arterial wall and VSMCs, which is modulated by VASN. Indeed, chronic administration of Ang II to young rats significantly activates MMP‐2 and diminishes the VASN expression to levels comparable to untreated older control rats. This review highlights and discusses the role played by VASN in mitigating fibrosis and calcification by alleviating TGF‐β1 activation and signaling in arterial walls and VSMCs. Understanding these molecular physical and functional interactions may pave the way for establishing VASN‐based therapeutic strategies to counteract adverse age‐associated cardiovascular remodeling, eventually reducing the risk of cardiovascular diseases.

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From Vascular Smooth Muscle Cells to Folliculogenesis: What About Vasorin?

Cited by 22 publications

References 23 publications

Vasorin deficiency leads to cardiac hypertrophy by targeting MYL7 in young mice

Vasorin deficiency leads to cardiac hypertrophy by targeting MYL7 in young mice

Lipoprotein Proteomics and Aortic Valve Transcriptomics Identify Biological Pathways Linking Lipoprotein(a) Levels to Aortic Stenosis

Enhanced vasorin signaling mitigates adverse cardiovascular remodeling

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